Studies will be continued on hemostatic mechanisms, their alteration in diseased states, and their relationship with other defense mechanisms of the body. Work will center on the activation of HF, on the relation between activated HF and fragments of HF known to activate plasma kallikrein, on the possible heterogeneity of normal AHF and on the effect of concanavalin A on normal platelets. These studies should aid in our understanding of the nature of the thrombotic process.